The ongoing work in our laboratory continues to be focused on two major goals, namely: 1) the identification of subjects susceptible to sudden cardiac death; and 2) development of measures for protecting those at risk of experiencing ventricular fibrillation. The critical hypothesis guiding our investigations is that transient risk factors may catapult the electrically unstable myocardium into ventricular fibrillation. These risk factors originate primarily from activity in the central nervous system. Our essential current goals in the animal laboratory are: 1) To determine the role of alpha-adrenergic receptors on ventricular vulnerability to fibrillation; 2) to define the role of coronary vasospasm in the genesis of ventricular arrhythmias; 3) To determine the mechanisms by which insulin exerts its potent antifibrillatory effect; 4) to examine the role of slow channels in the regulation of cardiac vulnerability in the conscious animal. Human investigations will emphasize work relating to identifying the factors which differentiate patients with malignant arrythmia on the basis of response to diverse antiarrhythmic drugs. We aim to continue systematizing the use of antiarrhythmic drugs including psychotropic agents. We shall also explore the role of coronary vasodilator drugs in subduing ventricular premature beats. An additional objective will be to develop noninvasive methods for defining myocardial electrical instability.